Madecassoside, a triterpenoid saponin isolated from Centella asiatica herbs, protects endothelial cells against oxidative stress

被引:52
作者
Bian, Difei [1 ]
Liu, Mei [1 ]
Li, Ying [1 ]
Xia, Yufeng [1 ]
Gong, Zhunan [2 ]
Dai, Yue [1 ]
机构
[1] China Pharmaceut Univ, Dept Pharmacol Chinese Mat Med, State Key Lab Nat Med, Nanjing 210009, Peoples R China
[2] Nanjing Normal Univ, Coll Life Sci, Ctr New Drug Res & Dev, Nanjing, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Madecassoside; Endothelial Cell; Oxidative Stress; Apoptosis; MAPK; REPERFUSION INJURY; INDUCED APOPTOSIS; DEATH; RAT; INHIBITION; CASPASE; MICE;
D O I
10.1002/jbt.21434
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
This study aimed to investigate the effect of madecassoside against oxidative stress-induced injury of endothelial cells. Hydrogen peroxide (H2O2, 500 mu mol/L) was employed as an inducer of oxidative stress in human umbilical vein endothelial cells (HUVECs). Cell apoptosis was detected by Hoechst 33258 staining and flow cytometry. Caspase-3 activity and mitochondria membrane potential were further examined. As a result, madecassoside (10, 30, 100 mu mol/L) could reverse morphological changes, elevate cell viability, increase glutathione levels, and decrease lactate dehydrogenase and malondialdehyde levels caused by H2O2 in a concentration-dependent manner. It attenuated apoptosis, preventing the activation of caspase-3 and the loss of mitochondria membrane potential, as well as the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in HUVECs. These data suggested that madecassoside could protect HUVECs from oxidative injury, which was probably achieved by inhibiting cell apoptosis via protection of mitochondria membranes and downregulation of the activation of caspase-3 and p38 MAPK. (c) 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:399406, 2012; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21434
引用
收藏
页码:399 / 406
页数:8
相关论文
共 23 条
[1]
Potential target sites to modulate vascular endothelial dysfunction: Current perspectives and future directions [J].
Balakumar, Pitchai ;
Kaur, Tajpreet ;
Singh, Manjeet .
TOXICOLOGY, 2008, 245 (1-2) :49-64
[2]
Madecassoside reduces ischemia-reperfusion injury on regional ischemia induced heart infarction in rat [J].
Bian, Guang-Xing ;
Li, Gui-Gui ;
Yang, Yun ;
Liu, Rui-Ting ;
Ren, Jian-Ping ;
Wen, Li-Qing ;
Guo, Shao-Ming ;
Lu, Qiu-Jun .
BIOLOGICAL & PHARMACEUTICAL BULLETIN, 2008, 31 (03) :458-463
[3]
Protein complexes activate distinct caspase cascades in death receptor and stress-induced apoptosis [J].
Bratton, SB ;
MacFarlane, M ;
Cain, K ;
Cohen, GM .
EXPERIMENTAL CELL RESEARCH, 2000, 256 (01) :27-33
[4]
Antioxidant properties of neohesperidin dihydrochalcone: Inhibition of hypochlorous acid-induced DNA strand breakage, protein degradation, and cell death [J].
Choi, Je-Min ;
Yoon, Byoung-Seok ;
Lee, Sang-Kyou ;
Hwang, Jae-Kwan ;
Ryang, Ryung .
BIOLOGICAL & PHARMACEUTICAL BULLETIN, 2007, 30 (02) :324-330
[5]
Fisher Mark, 2008, Rev Neurol Dis, V5 Suppl 1, pS4
[6]
REPERFUSION INJURY INDUCES APOPTOSIS IN RABBIT CARDIOMYOCYTES [J].
GOTTLIEB, RA ;
BURLESON, KO ;
KLONER, RA ;
BABIOR, BM ;
ENGLER, RL .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (04) :1621-1628
[7]
Development and validation of high-performance liquid chromatography/electrospray ionization mass spectrometry for assay of madecassoside in rat plasma and its application to pharmacokinetic study [J].
Han, Wen-Jing ;
Xia, Yu-Feng ;
Dai, Yue .
BIOMEDICAL CHROMATOGRAPHY, 2012, 26 (01) :26-32
[8]
Hotchkiss KA, 2002, MOL CANCER THER, V1, P1191
[9]
Oxidant signaling in vascular cell growth, death, and survival - A review of the roles of reactive oxygen species in smooth muscle and endothelial cell mitogenic and apoptotic signaling [J].
Irani, K .
CIRCULATION RESEARCH, 2000, 87 (03) :179-183
[10]
Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases [J].
Johnson, GL ;
Lapadat, R .
SCIENCE, 2002, 298 (5600) :1911-1912